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Psychological factors such as stress and depression have already been established as primary and secondary cardiovascular risk factors. More recently, the role of anxiety in increasing cardiac risk has also been studied. The underlying mechanisms of increased cardiac risk in panic disorder patients seem to reflect the direct and indirect effects of autonomic dysfunction, as well as behavioral risk factors associated with an unhealthy lifestyle. Implications of the comorbidity between panic and cardiovascular disease include higher morbidity, functional deficits, increased cardiovascular risk, and poor adherence to cardiac rehabilitation or exercise programs. This article probes the most recent evidence on the association between coronary artery disease, anxiety and panic disorder, and discusses the potential role of incorporating regular physical exercise and cognitive behavioral therapy in the treatment of this condition.

Our objective was to explore the dose-response relationship in patients with panic disorder and social anxiety disorder comorbidity (DSM-IV). After 1 week of no-drug washout, 36 such patients were assigned to a double-blind controlled comparison of the effects of 30 mg and 60 mg of tranylcypromine, and were followed up for 12 weeks. The main instrument used to measure the number of panic attacks was the Sheehan Panic and Anticipatory Anxiety Scale. The primary outcome measure for social anxiety disorder symptoms was the mean change from baseline in the Liebowitz Social Anxiety Scale (LSAS). After 12 weeks of treatment, panic attacks were reduced 69.6% from baseline in the 30-mg group (n=19) compared with a 74.8% reduction in the 60-mg group (n=17). Twelve patients (70.6%) of the higher dose group and 14 patients (68.4%) of the lower dose were completely free of panic attacks. There was no difference in efficacy between the tranylcypromine groups in the panic disorder symptoms. The 60-mg dose was more efficacious as measured by the LSAS scores, showing a significant difference in relation to the lower group. Mean change from baseline in LSAS total score (mean+/-SD) for 30-mg group was 17.9+/-14.7 and for the 60-mg group was 35.0+/-14.8. The social anxiety symptom scale showed a two-fold greater change with the 60-mg dose, and the 30-mg dose group could be considered the equivalent of a placebo control group. Tranylcypromine--60 mg daily--was found effective in the treatment of panic disorder and social anxiety disorder comorbidity.

OBJECTIVE: To determine the prevalence of anxiety and depression in patients complaining of chest pain who seek a chest pain unit attendance. INTRODUCTION: Patients arriving at a Chest Pain Unit may present psychiatric disorders not identified, isolated or co-morbid to the main illness, which may interfere in the patient prognosis. METHODOLOGY: Patients were assessed by the "Hospital Anxiety and Depression Scale" as a screening instrument wile following a systematized protocol to rule out the diagnosis of acute coronary syndrome and other potentially fatal diseases. Patients with 8 or more points in the scale were considered "probable case" of anxiety or depression. RESULTS: According to the protocol, 59 (45.4%) of 130 patients studied presented Chest Pain of Determined Cause, and 71 (54.6%) presented Chest Pain of Indefinite Cause. In the former group, in which 43 (33.1%) had acute coronary syndrome, 33.9% were probable anxiety cases and 30.5% depression cases. In the second group, formed by patients without acute coronary syndrome or any clinical conditions involving greater morbidity and mortality risk, 53.5% were probable anxiety cases and 25.4% depression. CONCLUSION: The high anxiety and depression prevalence observed may indicate the need for early and specialized approach to these disorders. When coronary arterial disease is present, this may decrease complications and shorten hospital stay. When psychiatric disorder appears isolated, is possible to reduce unnecessary repeated visits to emergency room and increase patient's quality of life.

Our aim was to observe the induction of anxiety symptoms and panic attacks by a caffeine challenge test in panic disorder (PD) patients (DSM-IV) and their healthy first-degree relatives. We randomly selected 25 PD patients, 27 healthy first-degree relatives of probands with PD, and 22 healthy volunteers with no family history of PD. In a randomized double-blind experiment performed over two occasions 7 days apart, 480 mg caffeine and a caffeine-free solution were administered in a coffee form. Using specific panic attack criteria, 52.0% (n=13) PD patients, 40.7% (n=11) first-degree relatives (chi2=1.81, df=1, P=0.179), and none of the control subjects had a panic attack after the test (chi2=51.7, df=2, P

Background: Mood disorders are considered related to anxiety disorders and their association may determine clinical course and prognosis. We aimed to describe with retrospective methodology the demographic, clinical, and treatment features in a group of panic disorder comorbid with bipolar I disorder (PD–BI) patients who were been treated for at least 3 year-period and compare them with bipolar I (BI) patients who were treated during the same period. Method: We compared the demographic and clinical data of 26 PD–BI, 28 BI, and 25 panic disorder (PD) outpatients without history of comorbidity with mood disorder were diagnosed and treated for at least 3 years in the Federal University of Rio de Janeiro. Results: PD group have a higher educational level, are more married, and are more economically active. In the PD–BI and BI patients the disorders started earlier. They also turn out to have an equivalent pattern in the presence of drug abuse episodes, moderate or severe depressive episodes, psychotic episodes, suicide attempts, maniac episodes, mixed episodes, use of fewer days of antidepressants and benzodiazepines, and use of more days of antipsychotics and mood stabilizers. The PD–BI and the BI groups had a higher frequency of depressive episodes and psychotic episodes. Limitations: It is a retrospective data description based on a naturalistic treatment. The sample has a small size and the some data could be different in a large sample. Conclusion: PD–BI patients have demographic, clinical and therapeutic features similar to BI and the data support its validation as a special severe bipolar I disorder subgroup. © 2007 Elsevier B.V. All rights reserved.

Our aim was to compare the demographic and clinical features of panic disorder (PD) patients with agoraphobia-DSM-IV-who had a panic attack after both an oral caffeine and the 35% carbon dioxide (CO2) challenge tests (responsive group) and compare them with PD patients who did not have a panic attack after both tests (non-responsive group). We examined 83 PD patients submitted to a 35% CO2 test and to an oral caffeine (480 mg) intake within 1 week interval. A panic attack was induced in 51 (61.4%) patients during the CO2 test (chi2=31.67, df=1, p

Background Schizobipolar disorder is considered related to both schizophrenia and bipolar disorder. We aimed to describe with retrospective methodology the demographic, clinical, and treatment features in a group of schizobipolar disorder patients who have been treated for at least a 5-year period and compare them with bipolar I and schizophrenic patients who were treated during the same period. Method We compared the demographic and clinical data of 61 schizobipolar, 57 bipolar I, and 55 schizophrenic outpatients who were diagnosed and treated for at least 5 years in the outpatient clinic in the Federal University of Rio de Janeiro. Results The schizobipolar disorder patients had a profile similar to the bipolar I patients but are significantly different from schizophrenic patients in educational level, marital status, occupation, drug and alcohol abuse episodes, presence of depressive, mixed and maniac episodes, family history of bipolar I and mood disorders, and use of medications. Only the age of onset, suicide attempts, and family history of suicide are not significantly different among the groups. The schizophrenic patients used antipsychotics for more days and the schizobipolar and bipolar I used more antidepressants and mood stabilizers. 37 (60.6%) schizobipolar patients had their diagnosis changed to bipolar disorder by their physician in different periods during the period studied. Limitations It is a retrospective data description based on a naturalistic treatment. The family history was collected from the patient and whenever possible from one first-degree relative. Conclusion Schizobipolar disorder patients have demographic, clinical and therapeutic features similar to bipolar I patients and data support its definite inclusion in the bipolar spectrum group.

Context In clinical practice, the importance of screening for anxiety and depression in patients with medical illness is highlighted. In many cases, the suicidal ideation makes up the framework of mental disorders, which may be exacerbated in these individuals. Objective To investigate the role of symptoms of mental disorders in the presence of suicidal ideation. Methods A total of 103 patients with diagnosis of coronary artery disease in cardiac treatment were interviewed for symptoms of anxiety and depression using the Beck Depression Inventory and Hospital Anxiety and Depression Scale. All patients were also analyzed for presence of suicidal ideation, wishes, attitude and suicidal plans using the Beck Suicidal Ideation Scale. The relationship between social and demographic variables and mental disturbances and the presence of suicidal ideation was assessed using chi-square test and coefficient of sperm. Logistic regression analysis was used to explain the change in the role of each of the variables in suicidal ideation. Results The results showed that predictors for suicidal ideation were isolated anxiety (B = 0.29; Wald 4.77; p = 0.03) with an odds ratio of 1.34 (CI 1.03–1.75) and isolated depression (B = 0.33; Wald 5.35; p = 0.02) with an odds ratio of 1.39 (CI 1.05–1.85). Frequencies of interaction depression and anxiety were higher among patients who were single, widowed and divorced. Chi-square test and the coefficient of sperm showed an association between marital status and suicidal ideation (χ2(2) = 9.17; p = 0.01). Conclusion Anxiety and depression are risk factors for isolated patients with suicidal ideation. Early clinical identification of mental disorders in patients with medical illness contributed to preventing the risk of suicide.

This article is a systematic review of the available literature on the benefits that cognitive behavioral therapy (CBT) offers patients with implanted cardioverter defibrillators (ICDs) and confirms its effectiveness. After receiving the device, some patients fear that it will malfunction, or they remain in a constant state of tension due to sudden electrical discharges and develop symptoms of anxiety and depression. A search with the key words “anxiety”, “depression”, “implantable cardioverter”, “cognitive behavioral therapy” and “psychotherapy” was carried out. The search was conducted in early January 2013. Sources for the search were ISI Web of Knowledge, PubMed, and PsycINFO. A total of 224 articles were retrieved: 155 from PubMed, 69 from ISI Web of Knowledge. Of these, 16 were written in a foreign language and 47 were duplicates, leaving 161 references for analysis of the abstracts. A total of 19 articles were eliminated after analysis of the abstracts, 13 were eliminated after full-text reading, and 11 articles were selected for the review. The collection of articles for literature review covered studies conducted over a period of 13 years (1998-2011), and, according to methodological design, there were 1 cross-sectional study, 1 prospective observational study, 2 clinical trials, 4 case-control studies, and 3 case studies. The criterion used for selection of the 11 articles was the effectiveness of the intervention of CBT to decrease anxiety and depression in patients with ICD, expressed as a ratio. The research indicated that CBT has been effective in the treatment of ICD patients with depressive and anxiety symptoms. Research also showed that young women represented a risk group, for which further study is needed. Because the number of references on this theme was small, further studies should be carried out.

Chest pain is often seen alongside with panic attacks. Moreover, panic disorder has been suggested as a risk factor for cardiovascular disease and even a trigger for acute coronary syndrome. Patients with coronary artery disease may have myocardial ischemia in response to mental stress, in which panic attack is a strong component, by an increase in coronary vasomotor tone or sympathetic hyperactivity setting off an increase in myocardial oxygen consumption. Indeed, coronary artery spasm was presumed to be present in cases of cardiac ischemia linked to panic disorder. These findings correlating panic disorder with coronary artery disease lead us to raise questions about the favorable prognosis of chest pain in panic attack. To investigate whether myocardial ischemia is the genesis of chest pain in panic attacks, we developed a myocardial perfusion study through research by myocardial scintigraphy in patients with panic attacks induced in the laboratory by inhalation of 35% carbon dioxide. In conclusion, from the data obtained, some hypotheses are discussed from the viewpoint of endothelial dysfunction and microvascular disease present in mental stress response.

Chest pain may be due benign diseases but often suggests an association with coronary artery disease, which justifies a quick search for medical care. However, some people have anxiety disorder with symptoms that resemble clearly an acute coronary syndrome. More specifically, during a panic attack an abrupt feeling of fear accompanied by symptoms such as breathlessness, palpitations and chest pain, makes patients believe they have a heart attack and confuse physicians about the diagnosis. The association between panic disorder and coronary artery disease has been extensively studied in recent years and, although some studies have shown anxiety disorders coexisting or increasing the risk of heart disease, one causal hypothesis is still missing. The aim of this systematic review is to present the various ways in which the scientific community has been investigating the relation between chest pain, panic disorder and coronary artery disease.

Objective: To systematically review the literature with regard to psychiatric disorders and quality of life in patients with an implantable cardioverter defibrillator. Data Sources: Research was conducted in 3 databases (ISI Web of Science, PubMed, and PsycINFO) using the terms implantable, cardioverter, defibrillator, quality of life, psych*, anxiety, and depression. Study Selection: The search yielded 1,399 references. Non-English and repeated references were excluded. After abstract analysis, 42 references were recovered for full-text reading, and 25 articles were selected for this review. Data Extraction: Research took place in April 2012, and no time restriction was placed on any of the database searches. Review or theoretical articles were excluded, and only clinical trials and epidemiologic studies were selected for this review. Results: A systematic review of the literature revealed mostly observational prospective cohort studies followed by cross-sectional observational studies and randomized clinical trials. Few studies included in the review were observational retrospective cohort or case-control studies. There are prominent signs and symptoms of anxiety and depression in patients with an implantable cardioverter defibrillator. Disorders include phobic anxiety, posttraumatic stress disorder, panic disorder, somatoform disorder, agoraphobia, and depression. Quality of life in the physical, social, and psychological domains is affected and is related to the intensity and the frequency of the device’s electrical discharge. Conclusions: Work regarding psychiatric comorbidity in patients with an implantable cardioverter defibrillator has shown that anxiety and depression are common. The patients and their families should be informed by their doctors that the presence of the device minimizes risk of sudden death and allows them to have a normal life.

The aim of this study was to conduct a systematic review of the literature regarding the prevalence of sexual dysfunction in patients with cardiovascular diseases. An article search of the ISI Web of Science and PubMed databases using the search terms "sexual dysfunction”, “cardiovascular diseases”, “coronary artery disease", “myocardial infarct" and “prevalence” was performed. In total, 893 references were found. Non-English-language and repeated references were excluded. After an abstract analysis, 91 references were included for full-text reading, and 24 articles that evaluated sexual function using validated instruments were selected for this review. This research was conducted in October 2012, and no time restrictions were placed on any of the database searches. Reviews and theoretical articles were excluded; only clinical trials and epidemiological studies were selected for this review. The studies were mostly cross-sectional, observational and case-control in nature; other studies used prospective cohort or randomized clinical designs. In women, all domains of sexual function (desire, arousal, vaginal lubrication, orgasm, sexual dissatisfaction and pain) were affected. The domains prevalent in men included erectile dysfunction and premature ejaculation and orgasm. Sexual dysfunction was related to the severity of cardiovascular disease. When they resumed sexual activity, patients with heart disease reported significant difficulty, including a lack of interest in sex, sexual dissatisfaction and a decrease in the frequency of sexual activity.

This long-term extension of an 8-week randomized, naturalistic study in patients with panic disorder with or without agoraphobia compared the efficacy and safety of clonazepam (n = 47) and paroxetine (n = 37) over a 3-year total treatment duration. Target doses for all patients were 2 mg/d clonazepam and 40 mg/d paroxetine (both taken at bedtime). This study reports data from the long-term period (34 months), following the initial 8-week treatment phase. Thus, total treatment duration was 36 months. Patients with a good primary outcome during acute treatment continued monotherapy with clonazepam or paroxetine, but patients with partial primary treatment success were switched to the combination therapy. At initiation of the long-term study, the mean doses of clonazepam and paroxetine were 1.9 (SD, 0.30) and 38.4 (SD, 3.74) mg/d, respectively. These doses were maintained until month 36 (clonazepam 1.9 [SD, 0.29] mg/d and paroxetine 38.2 [SD, 3.87] mg/d). Long-term treatment with clonazepam led to a small but significantly better Clinical Global Impression (CGI)-Improvement rating than treatment with paroxetine (mean difference: CGI-Severity scale -3.48 vs -3.24, respectively, P = 0.02; CGI-Improvement scale 1.06 vs 1.11, respectively, P = 0.04). Both treatments similarly reduced the number of panic attacks and severity of anxiety. Patients treated with clonazepam had significantly fewer adverse events than those treated with paroxetine (28.9% vs 70.6%, P < 0.001). The efficacy of clonazepam and paroxetine for the treatment of panic disorder was maintained over the long-term course. There was a significant advantage with clonazepam over paroxetine with respect to the frequency and nature of adverse events.

High-potency benzodiazepines, such as clonazepam, are frequently used in the treatment of panic disorder (PD) because of their rapid onset of action and good tolerability. However, there is concern about their potential to cause withdrawal symptoms. We aimed to develop a protocol for safely tapering off clonazepam in patients with PD who had been receiving treatment for at least 3 years. A specific scale for judging withdrawal was also developed, the Composite Benzodiazepine Discontinuation Symptom Scale. We selected 73 patients with PD who had been asymptomatic for at least 1 year and who wished to discontinue the medication. The trial consisted of a 4-month period of tapering and an 8-month follow-up period. The dosage of clonazepam was decreased by 0.5 mg per 2-week period until 1 mg per day was reached, followed by a decrease of 0.25 mg per week. The mean dosage at the start of tapering was 2.7 +/- 1.2 mg/d. In total, 51 (68.9%) of the patients were free of the medication after the 4 months of tapering according to the protocol, and 19 (26.0%) of the patients needed another 3 months to be free of medication. Clonazepam discontinuation symptoms were mostly mild and included mainly: anxiety, shaking/trembling/tremor, nausea/vomiting, insomnia/nightmares, excessive sweating, tachycardia/palpitations, headache, weakness, and muscle aches. The improvement in PD and general well-being was maintained during both the taper and follow-up phases. Clonazepam can be successfully discontinued without any major withdrawal symptoms if the dose is reduced gradually. We recommend reducing the dosage of clonazepam after intermediate-term use by 0.25 mg/wk.

Studies have demonstrated the vulnerability of anxiety disorder patients to challenge tests. Our aim was to observe if panic disorder (PD) patients and generalized social anxiety disorder (GSAD) and performance social anxiety disorder (PSAD) patients respond in a similar way to the induction of anxiety symptoms and panic attacks by an oral caffeine challenge test. We compared 28 PD patients, 25 GSAD patients, 19 PSAD, and 26 control subjects after a 480-mg caffeine test. The patients had not received psychotropic drugs for at least a 4-week period. In a randomized double-blind experiment performed in two occasions 7 days apart, 480 mg of caffeine and a caffeine-free solution were administered and anxiety scales were administered before and after each test. A panic attack was induced in 17 (60.7%) PD patients, 4 (16.0%) GSAD patients, and 10 (52.6%) PSAD patients, during the caffeine test. None of the control subjects had a panic attack after the caffeine intake. Neither patients nor any control subject had a panic attack after drinking the caffeine-free solution. Our data suggest that there is an association between PD and PSAD hyperreactivity to an oral caffeine challenge test. The PD and PSAD patients had a higher number of induced panic attacks, some specific anxiety symptoms, and a more severe anxiety response than GSAD patients and normal volunteers.

Objective:To describe with prospective methodology the therapeutic response to clonazepam or paroxetine in a 3-year treatment of panic disorder (PD).Methods:A total of 120 PD outpatients (DSM-IV) were openly treated with clonazepam or paroxetine for 8 weeks. Those who responded entered a 3-year follow-up. Demographic and clinical features were compared in the two groups.Results:Efficacy was evaluated by Intent to treat, last value carried forward. The Hamilton Scale for Anxiety (HAMA) did not differ between the groups at baseline and during the first two months. In the acute treatment phase and at the end of the long-term follow-up both groups had a significant and similar response - 86.8% of the clonazepam group and 73.0% of the paroxetine group had a complete remission of panic attacks. The mean dose for clonazepam was 1.9 ± 0.2 mg/day and for paroxetine 33.8 ± 9.8 mg/day. There was no difference in the scale scores, and the reduction in panic attacks from baseline to end-point did not differ significantly between the groups. The most common adverse events during treatment were tremor/shaking, nausea/vomiting, sexual dysfunction and appetite/weight change in the paroxetine group and drowsiness, sexual dysfunction and memory/concentration complains in the clonazepam group.Conclusion:PD patients using clonazepam or paroxetine had an equivalent response during acute and long term treatment. The patients using clonazepam had significantly less side effects than the paroxetine group.Acknowledgements: Brazilian Council for scientific and technological development (CNPq).Grant: 554411/2005-9.